Contrast-induced nephropathy (CIN) is a form of acute renal failure that occurs after the exposure to iodinated intravenous contrast, such as is used in cardiac catheterization procedures or CT scans. Individuals with baseline renal disease, diabetes, ongoing hypotension/heart failure/acute myocardial infarction, use of nephrotoxic drugs, or who are exposed to large amounts of contrast dye are at increased risk of this renal failure.
The natural history of Contrast-induced nephropathy is usually a transient decrease in renal function. In patients with severe baseline renal dysfunction however, the risk of proceeding to endstage renal disease (i.e requiring dialysis can be as high as 30%). Despite the usually transient nature of the Contrast-induced nephropathy episode itself, Contrast-induced nephropathy has been associated with increased longer term (1-2 year) morbidity and mortality. In addition, Contrast-induced nephropathy is also tightly associated with increased hospital stays and more acute cardiac events (such as pulmonary edema) during the index hospitalization.
The mechanism of contrast-induced kidney damage has been postulated to be a function of two separate processes: the first is a direct toxic effect of the dye to the tubular cells of the nephron unit. The second is a vasoconstrictive effect on the blood vessels of the renal medullary bed. In large part, the prior interventions attempted for the amelioration of CIN have focused on vasodilation in the renal beds—this included N-acetylcysteine, fenoldapam, theophylline, adenosine-receptor antagonists, calcium channel blockers and iloprost. None of these interventions has been definitively shown to decrease the incidence of CIN. N-Acetylcysteine (NAC) is nevertheless commonly used as it is generic, cheap and lacks toxicity. The current standard of care for those at risk of Contrast-induced nephropathy is to institute IV hydration 8-16 hours prior to exposure to the dyes.
Therefore, there is a clear need for improved therapy for the treatment and prevention of contrast-induced Nephropathy.